Nakata N, Kato H, Liu Y, Kogure K
Department of Neurology, Institute of Brain Diseases, Tohoku University School of Medicine, Sendai, Japan.
Neurosci Lett. 1992 Apr 13;138(1):86-8. doi: 10.1016/0304-3940(92)90478-p.
To elucidate the role of glutamate in the pathogenesis of altered neuronal vulnerability following sublethal ischemia, we measured the extracellular concentrations of glutamate in the gerbil hippocampus using a microdialysis technique. During and immediately after 3-min forebrain ischemia, the extracellular glutamate level showed a striking increase. However, pretreatment with 2-min ischemia 1 h or 4 days before secondary 3-min ischemia did not alter the amount of glutamate released. The result indicates that cumulative damage and tolerance, which take place after pretreatment with sublethal ischemia, are not induced through modification of the amount of glutamate released during secondary ischemia.
为了阐明谷氨酸在亚致死性缺血后神经元易损性改变的发病机制中的作用，我们使用微透析技术测量了沙鼠海马体中谷氨酸的细胞外浓度。在3分钟的前脑缺血期间及缺血后即刻，细胞外谷氨酸水平显著升高。然而，在第二次3分钟缺血前1小时或4天用2分钟缺血进行预处理，并未改变谷氨酸的释放量。结果表明，亚致死性缺血预处理后发生的累积损伤和耐受性，并非通过改变二次缺血期间谷氨酸的释放量而诱导产生。
